Publications
328 results found
Lenoir A, Whittaker H, Gayle A, et al., 2023, Mortality in non-exacerbating COPD: a longitudinal analysis of UK primary care data, Thorax, Vol: 78, Pages: 904-911, ISSN: 0040-6376
Introduction: Non-exacerbating patients with chronic obstructive pulmonary disease (COPD) are a less studied phenotype. We investigated clinical characteristics, mortality rates and causes of death among non-exacerbating compared with exacerbating patients with COPD.Methods: We used data from the Clinical Practice Research Datalink, Hospital Episode Statistics and Office for National Statistics between 1 January 2004 and 31 December 2018. Ever smokers with a COPD diagnosis with minimum 3 years of baseline information were included. We compared overall using Cox regression and cause-specific mortality rates using competing risk analysis, adjusted for age, sex, deprivation, smoking status, body mass index, GOLD stage and comorbidities. Causes of death were identified using International Classification of Diseases-10 codes.Results: Among 67 516 patients, 17.3% did not exacerbate during the 3-year baseline period. Mean follow-up was 4 years. Non-exacerbators were more likely to be male (63.3% vs 52.4%, p<0.001) and less often had a history of asthma (33.9% vs 43.6%, p<0.001) or FEV1<50% predicted (23.7 vs 31.8%) compared with exacerbators. Adjusted HR for overall mortality in non-exacerbators compared with exacerbators was 0.62 (95% CI 0.56 to 0.70) in the first year of follow-up and 0.87 (95% CI 0.83 to 0.91) thereafter. Non-exacerbating patients with COPD died less of respiratory causes than exacerbators (29.2% vs 40.3%) and more of malignancies (29.4% vs 23.4%) and cardiovascular diseases (26.2% vs 22.9%). HRs for malignant and circulatory causes of death were increased after the first year of follow-up.Discussion: In this primary care cohort, non-exacerbators showed distinct clinical characteristics and lower mortality rates. Non-exacerbators were equally likely to die of respiratory, malignant or cardiovascular diseases.
Mahmoud O, Granell R, Peralta GP, et al., 2023, Early-life and health behaviour influences on lung function in early adulthood, EUROPEAN RESPIRATORY JOURNAL, Vol: 61, ISSN: 0903-1936
Grosso A, Cerveri I, Cazzoletti L, et al., 2023, Inhaled corticosteroids and risk of osteoporosis in late-middle-aged subjects: a multicenter European cohort study., Minerva Med, Vol: 114, Pages: 15-21
BACKGROUND: Inhaled corticosteroids have been widely used for the regular treatment of asthma and chronic obstructive pulmonary diseases (COPD) over the past few decades. To date, studies investigating the effects of inhaled corticosteroids (ICS) on bone in populations including asthma and COPD patients, show conflicting results. The skeletal effects of ICS remain poorly understood. We assessed the association between ICS exposure and self-reported osteoporosis diagnosis in a European cohort study. METHODS: The analysis was carried out by using clinical and questionnaire data available for subjects participating in the ECRHS III (European Community Respiratory Health Survey) with age >55 years. RESULTS: Among the 3004 enrolled subjects, 245 were ICS users with an exposure ≥12 months. Osteoporosis was reported by 16 subjects in the ICS group (6.5%) and by 167 in the not exposed group (6.1%). The adjusted risk of osteoporosis in ICS users (≥12 months) was not greater in exposed subjects when compared with the unexposed ones (OR=1.02, 95CI%: 0.51, 2.03). The same result was observed even when considering in the analysis a longer exposure to the ICS use (≥36.5 months, the median ICS exposure for all subjects). History of COPD, use of oral corticosteroids, Body Mass Index, smoking and physical activity did not show any evidence of an association with osteoporosis. CONCLUSIONS: Our study did not show any significant association between long- term ICS use and self-reported diagnosis of osteoporosis in subjects aged >55 years. To explore the real effect of ICS on bone status, further studies are needed, especially in the long-term ICS exposure.
De Matteis S, Jarvis D, Darnton L, et al., 2022, Lifetime occupational exposures and chronic obstructive pulmonary disease risk in the UK Biobank cohort, Thorax, Vol: 77, Pages: 997-1005, ISSN: 0040-6376
BACKGROUND AND AIM: Occupational exposures are important, preventable causes of COPD. We previously found an increased risk of COPD among six occupations by analysing lifetime job histories and lung function data in the population-based UK Biobank cohort. We aimed to build on these findings and elucidate the underlying potential causal agents to focus preventive strategies. METHODS: We applied the ALOHA+job exposure matrix (JEM) based on the International Standard Classification of Occupations V.1988 codes, where exposure to 12 selected agents was rated as 0 (no exposure), 1 (low) or 2 (high). COPD was spirometrically defined as FEV1/FVC less than the lower limit of normal. We calculated semiquantitative cumulative exposure estimates for each agent by multiplying the duration of exposure and squared intensity. Prevalence ratio (PR) and 95% CI for COPD were estimated using robust Poisson regression adjusted for centre, sex, age, smoking and coexposure to JEM agents. Only associations confirmed among never-smokers and never-asthmatics were considered reliable. RESULTS: Out of 116 375 participants with complete job histories, 94 514 had acceptable/repeatable spirometry and smoking data and were included in the analysis. Pesticide exposure showed increased risk of COPD for ever exposure (PR=1.13, 95% CI 1.01 to 1.28) and high cumulative exposure (PR=1.32, 95% CI 1.12 to 1.56), with positive exposure-response trends (p trend=0.004), which were confirmed among never-smokers (p trend=0.005) and never-asthmatics (p trend=0.001). CONCLUSION: In a large population-based study, occupational exposure to pesticides was associated with risk of COPD. Focused preventive strategies for workers exposed to pesticides can prevent the associated COPD burden.
Moitra S, Carsin A-E, Abramson M, et al., 2022, Long-term effect of asthma on the development of obesity among adults: an international cohort study, ECRHS, Thorax, ISSN: 0040-6376
Adamson A, Portas L, Accordini S, et al., 2022, Communication of personalised disease risk by general practitioners to motivate smoking cessation in England: a cost-effectiveness and research prioritisation study, ADDICTION, Vol: 117, Pages: 1438-1449, ISSN: 0965-2140
Marcon A, Locatelli F, Dharmage SC, et al., 2021, The coexistence of asthma and COPD: risk factors, clinical history and lung function trajectories, EUROPEAN RESPIRATORY JOURNAL, Vol: 58, ISSN: 0903-1936
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- Citations: 9
Accordini S, Calciano L, Johannessen A, et al., 2021, Prenatal and prepubertal exposures to tobacco smoke in men may cause lower lung function in future offspring: a three-generation study using a causal modelling approach, EUROPEAN RESPIRATORY JOURNAL, Vol: 58, ISSN: 0903-1936
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- Citations: 13
Fuertes E, Jarvis D, 2021, The complex interplay between greenness and air pollution in respiratory health, Thorax, Vol: 76, Pages: 856-857, ISSN: 0040-6376
Archangelidi O, Sathiyajit S, Consonni D, et al., 2021, Cleaning products and respiratory health outcomes in occupational cleaners: a systematic review and meta-analysis, OCCUPATIONAL AND ENVIRONMENTAL MEDICINE, Vol: 78, Pages: 604-617, ISSN: 1351-0711
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- Citations: 11
Bui DS, Agusti A, Walters H, et al., 2021, Lung function trajectory and biomarkers in the Tasmanian Longitudinal Health Study, ERJ OPEN RESEARCH, Vol: 7
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- Citations: 2
Jarvelin M-R, Wielscher M, Amaral AF, et al., 2021, Genetic correlation and causal relationships between cardio-metabolic traits and lung function impairment, Genome Medicine, Vol: 13, Pages: 1-13, ISSN: 1756-994X
AbstractBackground: Associations of low lung function with features of poor cardio-metabolic health have been reported.It is, however, unclear whether these co-morbidities reflect causal associations, shared genetic heritability or areconfounded by environmental factors.Methods: We performed three analyses: (1) cardio-metabolic health to lung function association tests in NorthernFinland Birth cohort 1966, (2) cross-trait linkage disequilibrium score regression (LDSC) to compare geneticbackgrounds and (3) Mendelian randomisation (MR) analysis to assess the causal effect of cardio-metabolic traitsand disease on lung function, and vice versa (bidirectional MR). Genetic associations were obtained from the UKBiobank data or published large-scale genome-wide association studies (N > 82,000).Results: We observed a negative genetic correlation between lung function and cardio-metabolic traits and diseases.In Mendelian Randomisation analysis (MR), we found associations between type 2 diabetes (T2D) instruments andforced vital capacity (FVC) as well as FEV1/FVC. Body mass index (BMI) instruments were associated to all lung functiontraits and C-reactive protein (CRP) instruments to FVC. These genetic associations provide evidence for a causal effectof cardio-metabolic traits on lung function. Multivariable MR suggested independence of these causal effects fromother tested cardio-metabolic traits and diseases. Analysis of lung function specific SNPs revealed a potential causaleffect of FEV1/FVC on blood pressure.Conclusions: The present study overcomes many limitations of observational studies by using MendelianRandomisation. We provide evidence for an independent causal effect of T2D, CRP and BMI on lung functionwith some of the T2D effect on lung function being attributed to inflammatory mechanisms. Furthermore,this analysis suggests a potential causal effect of FEV1/FVC on blood pressure. Our detailed analysis of theinterplay between cardio-metabolic traits and impaired
Lam HCY, Jarvis D, 2021, Seasonal variation in total and pollen-specific immunoglobulin E levels in the European Community Respiratory Health Survey, CLINICAL AND EXPERIMENTAL ALLERGY, Vol: 51, Pages: 1085-1088, ISSN: 0954-7894
Probst-Hensch N, Jeong A, Stolz D, et al., 2021, Causal effects of body mass index on airflow obstruction and forced mid-expiratory flow: a mendelian randomization study taking interactions and age-specific instruments into consideration toward a life course perspective, Frontiers in Public Health, Vol: 9, Pages: 1-15, ISSN: 2296-2565
Obesity has complex links to respiratory health. Mendelian randomization (MR) enables assessment of causality of body mass index (BMI) effects on airflow obstruction and mid-expiratory flow. In the adult SAPALDIA cohort, recruiting 9,651 population-representative samples aged 18–60 years at baseline (female 51%), BMI and the ratio of forced expiratory volume in 1 second (FEV1) to forced vital capacity (FVC) as well as forced mid-expiratory flow (FEF25–75%) were measured three times over 20 follow-up years. The causal effects of BMI in childhood and adulthood on FEV1/FVC and FEF25–75% were assessed in predictive (BMI averaged over 1st and 2nd, lung function (LF) averaged over 2nd and 3rd follow-up; N = 2,850) and long-term cross-sectional models (BMI and LF averaged over all follow-ups; N = 2,728) by Mendelian Randomization analyses with the use of weighted BMI allele score as an instrument variable and two-stage least squares (2SLS) method. Three different BMI allele scores were applied to specifically capture the part of BMI in adulthood that likely reflects tracking of genetically determined BMI in childhood. The main causal effects were derived from models containing BMI (instrumented by BMI genetic score), age, sex, height, and packyears smoked as covariates. BMI interactions were instrumented by the product of the instrument (BMI genetic score) and the relevant concomitant variable. Causal effects of BMI on FEV1/FVC and FEF25–75% were observed in both the predictive and long-term cross-sectional models. The causal BMI- LF effects were negative and attenuated with increasing age, and stronger if instrumented by gene scores associated with childhood BMI. This non-standard MR approach interrogating causal effects of multiplicative interaction suggests that the genetically rooted part of BMI patterns in childhood may be of particular relevance for the level of small airway function and airflow obstruction later in life. The methodological re
Nerpin E, Ferreira DS, Weyler J, et al., 2021, Bronchodilator response and lung function decline: Associations with exhaled nitric oxide with regard to sex and smoking status, The World Allergy Organization Journal, Vol: 14, ISSN: 1939-4551
Background: Fractional exhaled nitric oxide (FeNO) is a marker of type-2 inflammation used both to support diagnosis of asthma and follow up asthma patients. The associations of FeNO with lung function decline and bronchodilator (BD) response have been studied only scarcely in large populations. Objectives: To study the association between FeNO and a) retrospective lung function decline over 20 years, and b) lung function response to BD among asthmatic subjects compared with non-asthmatic subjects and with regards to current smoking and sex. Methods: Longitudinal analyses of previous lung function decline and FeNO level at follow-up and cross-sectional analyses of BD response and FeNO levels in 4257 participants (651 asthmatics) from the European Community Respiratory Health Survey. Results: Among asthmatic subjects, higher percentage declines of FEV1 and FEV1/FVC were associated with higher FeNO levels (p = 0.001 for both) at follow-up. These correlations were found mainly among non-smoking individuals (p = 0.001) and females (p = 0.001) in stratified analyses.Percentage increase in FEV1 after BD was positively associated with FeNO levels in non-asthmatic subjects. Further, after stratified for sex and smoking separately, a positive association was seen between FEV1 and FeNO levels in non-smokers and women, regardless of asthma status. Conclusions: We found a relationship between elevated FeNO and larger FEV1 decline over 20 years among subjects with asthma who were non-smokers or women. The association between elevated FeNO levels and larger BD response was found in both non-asthmatic and asthmatic subjects, mainly in women and non-smoking subjects.
Tan DJ, Bui DS, Dai X, et al., 2021, Does the use of inhaled corticosteroids in asthma benefit lung function in the long-term? A systematic review and meta-analysis, EUROPEAN RESPIRATORY REVIEW, Vol: 30, ISSN: 0905-9180
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- Citations: 2
Russell MA, Dharmage S, Fuertes E, et al., 2021, The effect of physical activity on asthma incidence over 10 years: population-based study, ERJ Open Research, Vol: 7, ISSN: 2312-0541
Whittaker H, Bloom C, Morgan A, et al., 2021, Accelerated FEV1 decline and risk of cardiovascular disease and mortality in a primary care population of COPD patients, European Respiratory Journal, Vol: 57, ISSN: 0903-1936
Accelerated lung function decline has been associated with increased risk of cardiovascular disease (CVD) in a general population, but little is known about this association in chronic obstructive pulmonary disease (COPD). We investigated the association between accelerated lung function decline and CVD outcomes and mortality in a primary care COPD population.COPD patients without a history of CVD were identified in the Clinical Practice Research Datalink (CPRD-GOLD) primary care dataset (n=36 282). Accelerated FEV1 decline was defined using the fastest quartile of the COPD population's decline. Cox regression assessed the association between baseline accelerated FEV1 decline and a composite CVD outcome over follow-up (myocardial infarction, ischaemic stroke, heart failure, atrial fibrillation, coronary artery disease, and CVD mortality). The model was adjusted for age, gender, smoking status, BMI, history of asthma, hypertension, diabetes, statin use, mMRC dyspnoea, exacerbation frequency, and baseline FEV1 percent predicted.6110 (16.8%) COPD patients had a CVD event during follow-up; median length of follow-up was 3.6 years [IQR 1.7–6.1]). Median rate of FEV1 decline was –19.4 mL·year−1 (IQR, –40.5 to 1.9); 9095 (25%) patients had accelerated FEV1 decline (>–40.5 mL·year−1), 27 287 (75%) did not (≤ –40.5 mL·year−1). Risk of CVD and mortality was similar between patients with and without accelerated FEV1 decline (HRadj 0.98 [95%CI, 0.90–1.06]). Corresponding risk estimates were 0.99 (95%CI 0.83–1.20) for heart failure, 0.89 (95%CI 0.70–1.12) for myocardial infarction, 1.01 (95%CI 0.82–1.23) for stroke, 0.97 (95%CI 0.81–1.15) for atrial fibrillation, 1.02 (95%CI 0.87–1.19) for coronary artery disease, and 0.94 (95%CI 0.71–1.25) for CVD mortality. Rather, risk of CVD was associated with mMRC score ≥2 and ≥2 exacerbations in the year prior.CVD out
Lam H, Jarvis D, Fuertes E, 2021, Interactive effects of allergens and air pollution on respiratory health: A systematic review, Science of the Total Environment, Vol: 757, ISSN: 0048-9697
BackgroundStudies have demonstrated an adverse role of outdoor allergens on respiratory symptoms. It is unknown whether this effect is independent or synergistic of outdoor air pollutants.MethodsWe systematically reviewed all epidemiological studies that examined interaction effects between counts of outdoor airborne allergens (pollen, fungal spores) and air pollutants, on any respiratory health outcome in children and adults. We searched the MEDLINE, EMBASE and Scopus databases. Each study was summarized qualitatively and assessed for quality and risk of bias (International Prospective Register for Systematic Reviews, registration number CRD42020162571).ResultsThirty-five studies were identified (15 timeseries, eight case-crossovers, 11 panels and one cohort study), of which 12 reported a significant statistical interaction between an allergen and air pollutant. Eight interactions were related to asthma outcomes, including one on lung function measures and wheeze, three to medical consultations for pollinosis and one to allergic symptoms (nasal, ocular or bronchial). There was no consensus as to which allergen or air pollutant is more likely to interact. No study investigated whether interactions are stronger in atopic individuals.ConclusionDespite strong evidence from small experimental studies in humans, only a third of studies identified significant allergen-pollutant interactions using common epidemiological study designs. Exposure misclassification, failure to examine subgroups at risk, inadequate statistical power or absence of population-level effects are possible explanations.
Lytras T, Beckmeyer-Borowko A, Kogevinas M, et al., 2021, Cumulative Occupational Exposures and Lung-Function Decline in Two Large General-Population Cohorts, ANNALS OF THE AMERICAN THORACIC SOCIETY, Vol: 18, Pages: 238-246, ISSN: 1546-3222
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- Citations: 7
Fuertes E, Marcon A, Potts L, et al., 2021, Health Impact assessment to predict the impact of tobacco price increases on COPD burden in Italy, England and Sweden, Scientific Reports, Vol: 11, ISSN: 2045-2322
Raising tobacco prices effectively reduces smoking, the main risk factor for chronic obstructive pulmonary disease (COPD). Using the Health Impact Assessment tool “DYNAMO-HIA”, this study quantified the reduction in COPD burden that would occur in Italy, England and Sweden over 40 years if tobacco prices were increased by 5%, 10% and 20% over current local prices, with larger increases considered in secondary analyses. A dynamic Markov-based multi-state simulation modelling approach estimated the effect of changes in smoking prevalence states and probabilities of transitioning between smoking states on future smoking prevalence, COPD burden and life expectancy in each country. Data inputs included demographics, smoking prevalences and behaviour and COPD burden from national data resources, large observational cohorts and datasets within DYNAMO-HIA. In the 20% price increase scenario, the cumulative number of COPD incident cases saved over 40 years was 479,059 and 479,302 in Italy and England (populous countries with higher smoking prevalences) and 83,694 in Sweden (smaller country with lower smoking prevalence). Gains in overall life expectancy ranged from 0.25 to 0.45 years for a 20 year-old. Increasing tobacco prices would reduce COPD burden and increase life expectancy through smoking behavior changes, with modest but important public health benefits observed in all three countries.
Lam C, Turner P, Hemming D, et al., 2021, Seasonality of food-related anaphylaxis admissions and associations with temperature and pollen levels, Journal of Allergy and Clinical Immunology: In Practice, Vol: 9, Pages: 518-520.e2, ISSN: 2213-2198
Whittaker H, Pimenta J, Jarvis D, et al., 2020, Characteristics associated with accelerated lung function decline in a primary care population with chronic obstructive pulmonary disease, International Journal of COPD, Vol: 2020, Pages: 3079-3091, ISSN: 1176-9106
Background: Estimates for lung function decline in chronic obstructive pulmonary disease (COPD) have differed by study setting and have not been described in a UK primary care population.Purpose: To describe rates of FEV1 and FVC decline in COPD and investigate characteristics associated with accelerated decline.Patients and Methods: Current/ex-smoking COPD patients (35 years+) who had at least 2 FEV1 or FVC measurements ≥ 6 months apart were included using Clinical Practice Research Datalink. Patients were followed up for a maximum of 13 years. Accelerated rate of lung function decline was defined as the fastest quartile of decline using mixed linear regression, and association with baseline characteristics was investigated using logistic regression.Results: A total of 72,683 and 50,649 COPD patients had at least 2 FEV1 or FVC measurements, respectively. Median rates of FEV1 and FVC changes or decline were − 18.1mL/year (IQR: − 31.6 to − 6.0) and − 22.7mL/year (IQR: − 39.9 to − 6.7), respectively. Older age, high socioeconomic status, being underweight, high mMRC dyspnoea and frequent AECOPD or severe AECOPD were associated with an accelerated rate of FEV1 and FVC decline. Current smoking, mild airflow obstruction and inhaled corticosteroid treatment were additionally associated with accelerated FEV1 decline whilst women, sputum production and severe airflow obstruction were associated with accelerated FVC decline.Conclusion: Rate of FEV1 and FVC decline was similar and showed similar heterogeneity. Whilst FEV1 and FVC shared associations with baseline characteristics, a few differences highlighted the importance of both lung function measures in COPD progression. We identified important characteristics that should be monitored for disease progression.
Douglas P, Fecht D, Jarvis D, 2020, Characterising populations living close to intensive farming and composting facilities in England, Frontiers of Environmental Science and Engineering, Vol: 15, Pages: 1-13, ISSN: 2095-2201
Bioaerosol exposure has been linked to adverse respiratory conditions. Intensive farming and composting facilities are important anthropogenic sources of bioaerosols. We aimed to characterise populations living close to intensive farming and composting facilities. We also infer whether the public are becoming more concerned about anthropogenic bioaerosol emissions, using reports of air pollution related incidents attributed to facilities. We mapped the location of 1,257 intensive farming and 310 composting facilities in England in relation to the resident population and its characteristics (sex and age), area characteristics (deprivation proxy and rural/urban classification) and school locations stratified by pre-defined distance bands from these bioaerosol sources. We also calculated the average number of air pollution related incidents per year per facility. We found that more than 16% of the population and 15% of schools are located within 4,828 m of an intensive farming facility or 4,000 m of a composting facility; few people (0.01 %) live very close to these sites and tend to be older people. Close to composting facilities, populations are more likely to be urban and more deprived. The number of incidents were attributed to a small proportion of facilities; population characteristics around these facilities were similar. Results indicate that populations living near composting facilities (particularly>250 to ⩽ 4,000 m) are mostly located in urban areas (80%–88% of the population), which supports the need for more community health studies to be conducted. Results could also be used to inform risk management strategies at facilities with higher numbers of incidents.
Accordini S, Marchetti P, Marcon A, et al., 2020, Trends of asthma incidence over 80 years in Europe: preliminary results from the Ageing Lungs in European Cohorts (ALEC) study, Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936
Alif S, Benke G, Kromhout H, et al., 2020, Occupational Exposures and Incidence of ASTHMA Over Two Decades in the ECRHS, Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936
Allinson J, Afzal S, Colak Y, et al., 2020, Collating data from major European population studies - The CADSET (Chronic airway disease early stratification) clinical research collaboration, Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936
Peralta GP, Granell R, Bedard A, et al., 2020, The mediating role of C-reactive protein (CRP) and insulin resistance in the association of mid-childhood fat mass and airflow limitation at 15 years, Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936
van der Plaat DA, Minelli C, Jarvis DL, et al., 2020, Polycystic ovary syndrome and lung function: a Mendelian randomization study, American Journal of Obstetrics and Gynecology, Vol: 223, Pages: 455-457, ISSN: 0002-9378
Bédard A, Carsin A-E, Fuertes E, et al., 2020, Physical activity and lung function - cause or consequence?, PLoS One, Vol: 15, ISSN: 1932-6203
Concerns exist that the positive association of physical activity with better lung function, which has been suggested in previous longitudinal studies in smokers, is due to reverse causation. To investigate this, we applied structural equation modeling (SEM), an exploratory approach, and marginal structural modeling (MSM), an approach from the causal inference framework that corrects for reverse causation and time-dependent confounding and estimates causal effects, on data from participants in the European Community Respiratory Health Survey (ECRHS, a multicentre European cohort study initiated in 1991–1993 with ECRHS I, and with two follow-ups: ECRHS II in 1999–2003, and ECRHS III in 2010–2014). 753 subjects who reported current smoking at ECRHS II, with repeated data on lung function at ECRHS I, II and III, physical activity at ECRHS II and III, and potential confounders at ECRHS I and II, were included in the analyses. SEM showed positive associations between physical activity and lung function in both directions. MSM suggested a protective causal effect of physical activity on lung function (overall difference in mean β (95% CI), comparing active versus non-active individuals: 58 mL (21–95) for forced expiratory volume in one second and 83 mL (36–130) for forced vital capacity). Our results suggest bi-directional causation and support a true protective effect of physical activity on lung function in smokers, after accounting for reverse causation and time-dependent confounding.
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